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Li, W., & Wang, Y. (2023). Stress granules: Potential therapeutic targets for infectious and inflammatory diseases. Frontiers in immunology, Volume 14 - 2023. 
Added by: Dr. Enrique Feoli (07/05/2025, 00:49)   Last edited by: Dr. Enrique Feoli (07/05/2025, 01:15)
Resource type: Journal Article
DOI: 10.3389/fimmu.2023.1145346
ID no. (ISBN etc.): 1664-3224
BibTeX citation key: Li2023
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Categories: BioAcyl Corp
Subcategories: Constitutive innate immunity
Creators: Li, Wang
Collection: Frontiers in immunology
Views: 2/15
Abstract
Eukaryotic cells are stimulated by external pressure such as that derived from heat shock, oxidative stress, nutrient deficiencies, or infections, which induce the formation of stress granules (SGs) that facilitates cellular adaptation to environmental pressures. As aggregated products of the translation initiation complex in the cytoplasm, SGs play important roles in cell gene expression and homeostasis. Infection induces SGs formation. Specifically, a pathogen that invades a host cell leverages the host cell translation machinery to complete the pathogen life cycle. In response, the host cell suspends translation, which leads to SGs formation, to resist pathogen invasion. This article reviews the production and function of SGs, the interaction between SGs and pathogens, and the relationship between SGs and pathogen-induced innate immunity to provide directions for further research into anti-infection and anti-inflammatory disease strategies.
Added by: Dr. Enrique Feoli  Last edited by: Dr. Enrique Feoli
Notes

 The main components of SGs and the factors that induce SGs formation. SGs comprise the following 7 components: (1) mRNAs that are protected from degradation. (2) TIFs targeting mRNAs, such as eIF4E, elF3, PABPC1, p-elF2α and elF5a; (3) RNA-binding proteins (RBPs) that regulate translation and protect mRNA stability, such as TIA-1, TIAR, HuR/ELAVL1, FMRP and PUM1; (4) mRNA metabolism-related proteins, such as G3BP1, G3BP2, DDX6, PMR1, SMN, STAU1, DHX36, caprin-1, ZBP1, HDAC6 and ADAR1; (5) signaling proteins, such as mTOR, RACK1 and TRAF; (6) expression products of interferon-stimulated genes (ISGs), such as PKR, RIG-I, MDA5 and LGP2, RNase L and OAS; and (7) regulatory proteins in SGs formation, such as APOBEC3G, Ago2, BRF1, DDX3, FAST and TTP.

Eight factors induce SGs formation: (1) endogenous stressors, such as low-level nutrients, hypoxia, and osmotic shock; (2) environmental stressors, such as heat shock, UV radiation, arsenic compounds, H2O2, menadione, diethyl maleate (DEM), paraquat, and brain ischemia; (3) overexpressed G3BP1, TIA-1, TZAR, TTP, FMRP, CPEB, SMN, DYRK3, tRNA fragments, and Aβ42; (4) translation modulators, such as puromycin, salubrinal, cycloheximide, emetine, and ISRIB; (5) proteasome inhibitors, such as MG 132 and lactacystin; (6) ER stressors, such as DTT and thapsigargin; (7) mitochondrial poisons, such as FCCP, clotrimazole, and sodium azide; and (8) other compounds, such as sorbitol, pateamine A, hippuristanol, silvestrol, 15d-prostaglandin J2 (15d-PGJ2); prostaglandin A1, selenite, salicylate, and A769662.


Added by: Dr. Enrique Feoli  Last edited by: Dr. Enrique Feoli
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